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• W2050278313 startingPage "651" @default.
• W2050278313 abstract "Intracellular calcium ([Ca2+]i) plays a pivotal role in neuronal ischemia. The aim of the present study was to investigate the routes of Ca2+ entry during non-excitotoxic oxygen and glucose deprivation (OGD) in acutely dissociated rat CA1 neurons. During OGD the fluo-3/fura red ratio reflecting [Ca2+]i increased rapidly and irreversibly. [Ca2+]i increased to the same degree in Ca2+ depleted medium, and also when both the ryanodine receptors (RyR) and the inositol 1,4,5-trisphosphate (IP3) receptors were blocked. When the endoplasmic reticulum (ER) Ca2+ stores were emptied with thapsigargin no increase in [Ca2+]i was observed independent of extracellular Ca2+. The OGD induced Ca2+ deregulation in isolated CA1 neurons is not prevented by removing Ca2+, or by blocking the IP3– or RyR receptors. However, when SERCA was blocked, no increase in [Ca2+]i was observed suggesting that SERCA dysfunction represents an important mechanism for ischemic Ca2+ overload." @default.
• W2050278313 created "2016-06-24" @default.
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• W2050278313 date "2005-05-01" @default.
• W2050278313 modified "2023-10-14" @default.
• W2050278313 title "Endoplasmic Reticulum Dysfunction and Ca2+ Deregulation in Isolated CA1 Neurons during Oxygen and Glucose Deprivation" @default.
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• W2050278313 doi "https://doi.org/10.1007/s11064-005-2753-6" @default.
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